Ginsenoside Rk1 induces cell death through ROS-mediated PTEN/PI3K/Akt/mTOR signaling pathway in MCF-7 cells

Journal of Functional Foods

Daidi Fan¹  Yinan Hong² 

[1] Shaanxi R&D Center of Biomaterials and Fermentation Engineering, School of Chemical Engineering, Northwest University, 229 Taibai North Road, Xi’an, Shaanxi 710069, China;Shaanxi Key Laboratory of Degradable Biomedical Materials, School of Chemical Engineering, Northwest University, 229 Taibai North Road, Xi’an, Shaanxi 710069, China;

关键词: Ginsenoside Rk1;    MCF-7 cells;    Apoptosis;    ROS;    PTEN/PI3K/Akt/mTOR pathway;   

DOI  :  

来源: DOAJ

【 摘 要 】

Ginsenosides have been reported to possess pharmacological effects, such as antioxidative, anti-inflammatory and antitumor effects. Nevertheless, little has been reported about the anti-breast cancer effects of ginsenoside Rk1 (Rk1). In this work, we explored the anti-breast cancer effects of Rk1. The results suggested that Rk1 suppressed cell growth, colony formation, and triggered S phase arrest. Rk1 also triggered ROS overproduction, reduced mitochondrial membrane potential and induced apoptosis. Moreover, the PTEN/PI3K/Akt/mTOR pathway was involved in Rk1-induced apoptosis. Treatment with Z-VAD-FMK, LY294002 and N-acetylcysteine further illustrated that Rk1 induced apoptosis in MCF-7 cells through ROS-mediated PTEN/PI3K/Akt/mTOR signaling pathway. Furthermore, in xenograft nude mice model, Rk1 treatment dramatically suppressed tumor growth and caused no obvious injuries to major organs. Taken together, the results of this study demonstrated, for the first time, the anticancer efficacy and mechanism of Rk1 in MCF-7 cells, providing basic evidence supporting Rk1 as a potential anti-breast cancer agent.

【 授权许可】

Unknown